Fig. 5.

DKO mice demonstrate impaired pro-survival protein phosphorylation in the striatum acutely following 5.0 g/kg ethanol administration. (A) By 1 hour after ethanol, phosphorylation of IRS-1 is significantly impaired in DKO mice compared to WT ethanol (**, p < 0.05) and DKO saline controls (*, p < 0.05) as measured by immunoblot analysis. (B) By 2 hours after ethanol, phosphorylation of AKT is significantly impaired in WT and DKO mice compared to WT and DKO saline controls (*, p < 0.05), respectively as measured by immunoblot analysis. At 3 hours after ethanol treatment, levels of phosphorylated AKT are still reduced in WT mice compared to saline controls (*, p < 0.05), DKO mice demonstrate levels that are significantly reduced compared to WT ethanol controls (**, p < 0.05). (C) By 2–3 hours after ethanol, phosphorylation of ERK (p44) is significantly impaired in DKO mice compared to WT ethanol (**, p < 0.05) and DKO saline controls (*, p < 0.05) as measured by immunoblot analysis. By 2 hours after ethanol, phosphorylation of ERK (p42) is significantly impaired in WT and DKO mice compared to WT and DKO saline controls (*, p < 0.05), respectively as measured by immunoblot analysis. At 3 hours after ethanol treatment, levels of phosphorylated ERK (p42) in WT mice had returned to controls levels, however, DKO mice demonstrate levels that are significantly reduced compared to WT ethanol controls (**, p < 0.05) and DKO saline controls (*, p < 0.05).